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  • Title: Evaluation of negative inotropic and antiarrhythmic effects of class 1 antiarrhythmic drugs.
    Author: Nawada T, Tanaka Y, Hirai S, Hisatome I, Hasegawa J, Kotake H, Mashiba H.
    Journal: Int J Clin Pharmacol Ther; 1994 Jul; 32(7):347-55. PubMed ID: 7952796.
    Abstract:
    The effects of 6 class 1 antiarrhythmic drugs (aprindine, cibenzoline, disopyramide, lidocaine, pirmenol, and quinidine) on myocardial action potential, its maximal upstroke velocity (Vmax) and isometric contractile force were evaluated by electrophysiological techniques. All the class 1 antiarrhythmic drugs examined had dose-dependent negative inotropic effects. The inhibitory effects on contractile force (Fc) was compared with the inhibitory effects on sodium channels under fast response. This ratio was indicated by IC50 Vmax/IC50Fc, and when evaluated and arranged in order of descending magnitude, these were the results: pirmenol, disopyramide, lidocaine, quinidine, cibenzoline and aprindine. The negative inotropic effects and the effects on action potential duration induced by these antiarrhythmic drugs were independent of each other; it had been found that classification of the drugs according to their effects on action potential duration did not provide sufficient information about negative inotropic effects. Class 1 antiarrhythmic drugs can be divided into 3 groups depending on the regression pattern of myocardial contractile force and the Vmax of action potentials under fast response and slow response. Drugs, whose inhibitory effects on sodium channels, are the main cause of negative inotropic effects. Drugs, whose inhibitory effects on calcium channels, are the main cause of negative inotropic effects. Drugs for which it is difficult to determine whether sodium channel or calcium channel blockade contributes more to their negative inotropic effects.
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